Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-11-30
pubmed:abstractText
Although many previous reports have examined the function of prostaglandin E(2) (PGE(2)) in the migration and proliferation of various cell types, the role of the actin cytoskeleton in human mesenchymal stem cells (hMSCs) migration and proliferation has not been reported. The present study examined the involvement of profilin-1 (Pfn-1) and filamentous-actin (F-actin) in PGE(2)-induced hMSC migration and proliferation and its related signal pathways. PGE(2) (10(-6)?M) increased both cell migration and proliferation, and also increased E-type prostaglandin receptor 2 (EP2) mRNA expression, ?-arrestin-1 phosphorylation, and c-Jun N-terminal kinase (JNK) phosphorylation. Small interfering RNA (siRNA)-mediated knockdown of ?-arrestin-1 and JNK (-1, -2, -3) inhibited PGE(2)-induced growth of hMSCs. PGE(2) also activated Pfn-1, which was blocked by JNK siRNA, and induced F-actin level and organization. Downregulation of Pfn-1 by siRNA decreased the level and organization of F-actin. In addition, specific siRNA for TRIO and F-actin-binding protein (TRIOBP) reduced the PGE(2)-induced increase in hMSC migration and proliferation. Together, these experimental data demonstrate that PGE(2) partially stimulates hMSCs migration and proliferation by interaction of Pfn-1 and F-actin via EP2 receptor-dependent ?-arrestin-1/JNK signaling pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1097-4652
pubmed:author
pubmed:copyrightInfo
© 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
226
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
559-71
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Interaction of profilin-1 and F-actin via a ?-arrestin-1/JNK signaling pathway involved in prostaglandin E(2)-induced human mesenchymal stem cells migration and proliferation.
pubmed:affiliation
Department of Veterinary Physiology, College of Veterinary Medicine, Biotherapy Human Resources Center (BK21), Chonnam National University, Gwangju, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't